Caloric restriction ameliorates high-fat diet induced cognitive deficits through attenuating neuroinflammation<i>via</i>the TREM2-PI3K/AKT signaling pathway

Wang, Rui; Zhou, Zhi; Wang, Dong-Fan; Zhao, Qingqing; Zhang, Changcheng; Liu, Chaoqi; Zhao, Haixia; Yuan, Chengfu; Yuan, Ding; Wang, Ting

doi:10.1039/d0fo02946g

Cited by 16 publications

(4 citation statements)

References 71 publications

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“…HFD, correlated with cognitive impairments and neurological deficits, increases the risk of neurological disorders like Alzheimer's disease later in life 165,166 . HFD inhibits CREB phosphorylation in the hippocampus and downregulates the expression of CREB target genes (Bdnf, nNOS, Sirt1, Egr3, and RelA genes).…”

Section: Exosome Therapy Enhances Neurorestoration Concurring With Co...mentioning

confidence: 99%

“…HFD, correlated with cognitive impairments and neurological deficits, increases the risk of neurological disorders like Alzheimer's disease later in life. 165 , 166 HFD inhibits CREB phosphorylation in the hippocampus and downregulates the expression of CREB target genes (Bdnf, nNOS, Sirt1, Egr3, and RelA genes). Still, intranasal administration of NSC‐derived exosomes epigenetically restores the transcription of these genes by the recruitment of CREB and improves recognition and spatial memory of animals analyzed with NORT and object place recognition (OPR) test.…”

Section: Exosome Therapy Enhances Neurorestoration Concurring With Co...mentioning

confidence: 99%

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Exosomes as a therapeutic tool to promote neurorestoration and cognitive function in neurological conditions: Achieve two ends with a single effort

Fallahi,

Zangbar,

Farajdokht

et al. 2024

CNS Neurosci Ther

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Exosomes possess a significant role in intercellular communications. In the nervous system, various neural cells release exosomes that not only own a role in intercellular communications but also eliminate the waste of cells, maintain the myelin sheath, facilitate neurogenesis, and specifically assist in normal cognitive function. In neurological conditions including Parkinson's disease (PD), Alzheimer's disease (AD), traumatic brain injury (TBI), and stroke, exosomal cargo like miRNAs take part in the sequela of conditions and serve as a diagnostic tool of neurological disorders, too. Exosomes are not only a diagnostic tool but also their inhibition or administration from various sources like mesenchymal stem cells and serum, which have shown a worthy potential to treat multiple neurological disorders. In addition to neurodegenerative manifestations, cognitive deficiencies are an integral part of neurological diseases, and applying exosomes in improving both aspects of these diseases has been promising. This review discusses the status of exosome therapy in improving neurorestorative and cognitive function following neurological disease.

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Section: Exosome Therapy Enhances Neurorestoration Concurring With Co...mentioning

confidence: 99%

Section: Exosome Therapy Enhances Neurorestoration Concurring With Co...mentioning

confidence: 99%

Exosomes as a therapeutic tool to promote neurorestoration and cognitive function in neurological conditions: Achieve two ends with a single effort

Fallahi,

Zangbar,

Farajdokht

et al. 2024

CNS Neurosci Ther

View full text Add to dashboard Cite

show abstract

“…Various strategies, such as nutrition, anti-obesity drugs and exercise, have been tested to assess their effects on mitigating cognitive and mood-related impairments induced by HFD ( Park et al, 2019 ; Ruegsegger et al, 2019 ; Nuzzo et al, 2020 ; Wang et al, 2021 ). Expectedly, most of these treatments demonstrated improvement in obesity-related metabolic abnormalities, including reduction of body weight, fat content, serum glucose level, and insulin resistance to varying extents, alongside their diverse influences on the CNS.…”

Section: Introductionmentioning

confidence: 99%

Probucol mitigates high-fat diet-induced cognitive and social impairments by regulating brain redox and insulin resistance

Wu,

Yang,

Huang

et al. 2024

Front. Neurosci.

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Probucol has been utilized as a cholesterol-lowering drug with antioxidative properties. However, the impact and fundamental mechanisms of probucol in obesity-related cognitive decline are unclear. In this study, male C57BL/6J mice were allocated to a normal chow diet (NCD) group or a high-fat diet (HFD) group, followed by administration of probucol to half of the mice on the HFD regimen. Subsequently, the mice were subjected to a series of behavioral assessments, alongside the measurement of metabolic and redox parameters. Notably, probucol treatment effectively alleviates cognitive and social impairments induced by HFD in mice, while exhibiting no discernible influence on mood-related behaviors. Notably, the beneficial effects of probucol arise independently of rectifying obesity or restoring systemic glucose and lipid homeostasis, as evidenced by the lack of changes in body weight, serum cholesterol levels, blood glucose, hyperinsulinemia, systemic insulin resistance, and oxidative stress. Instead, probucol could regulate the levels of nitric oxide and superoxide-generating proteins, and it could specifically alleviate HFD-induced hippocampal insulin resistance. These findings shed light on the potential role of probucol in modulating obesity-related cognitive decline and urge reevaluation of the underlying mechanisms by which probucol exerts its beneficial effects.

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“…Various strategies, such as nutrition, anti-obesity drugs and exercise, have been tested to assess their effects in mitigating cognitive and mood impairments induced by HFD (26)(27)(28)(29). As anticipated, most of these treatments demonstrated improvement in obesityrelated metabolic abnormalities, including reductions in body weight, fat content, serum glucose levels, and insulin resistance to varying extents, alongside their diverse impacts on CNS.…”

Section: Introductionmentioning

confidence: 99%

Probucol mitigates high-fat diet-induced cognitive and social impairments through disruption of redox-inflammation association

Wu,

Huang,

Yang

et al. 2023

Preprint

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Obesity and its detrimental metabolic consequences are commonly recognized as risk factors for impairments in the central nervous system (CNS). However, the direct link between metabolic abnormalities and brain functions during high-fat feeding remains unclear. Here, we show that treatment with probucol, a cholesterol-lowering drug, counteracts the cognitive and social impairments induced by a high-fat diet in mice, while having no effect on mood disorders. Unexpectedly, the beneficial effects of probucol do not result from rectifying obesity or restoring glucose and lipid homeostasis, as evidenced by the lack of change in body weight, blood glucose and serum cholesterol levels. Interestingly, high-fat feeding led to association among the levels of redox factors, including oxidized low-density lipoprotein, glutathione and malondialdehyde, as well as a significant negative correlation between malondialdehyde levels and behavioral performance. Probucol treatment interrupts these linkages and differentially regulates the proteins for the generation of reactive oxygen species and reactive nitrogen species in the brain. These findings prompt a reconsideration of the mechanism of action of probucol, as well as the roles of altered metabolic profiles and free radicals in brain function.

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Caloric restriction ameliorates high-fat diet induced cognitive deficits through attenuating neuroinflammationviathe TREM2-PI3K/AKT signaling pathway

Abstract: Prolonged high-fat diet (HFD) feeding impairs cognitive function in rodents. However, the mechanism of caloric restriction (CR) remedying HFD induced cognitive dysfunction remains elusive. In the present study，we investigated the...

Cited by 16 publications

References 71 publications

Exosomes as a therapeutic tool to promote neurorestoration and cognitive function in neurological conditions: Achieve two ends with a single effort

Exosomes as a therapeutic tool to promote neurorestoration and cognitive function in neurological conditions: Achieve two ends with a single effort

Probucol mitigates high-fat diet-induced cognitive and social impairments by regulating brain redox and insulin resistance

Probucol mitigates high-fat diet-induced cognitive and social impairments through disruption of redox-inflammation association

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